Acute Respiratory Emergencies · 2019-07-19 · Pneumothorax PTE Aspiration ... Modern diagnostic pathway uses:- clinical probability D-dimer assay CTPA. Pulmonary Embolism Diagnostic

Acute Respiratory Emergencies

Acute Respiratory Emergencies

Martin JohnsonConsultant PhysicianGartnavel / Western

Martin JohnsonConsultant PhysicianGartnavel / Western

SummarySummary

What to expect - what are the common respiratory emergencies?How to recognise the problem?How to manage the problem?

What to expect - what are the common respiratory emergencies?How to recognise the problem?How to manage the problem?

Relative Frequency of Medical EmergenciesRelative Frequency of Medical Emergencies

The burden of lung disease. 2nd Edition BTS 2006

Relative Frequency of Respiratory Emergencies

Relative Frequency of Respiratory Emergencies

The burden of lung disease. 2nd Edition BTS 2006

Immediate AssessmentImmediate Assessment

How to recognise the problem?

How to recognise the problem?

HistoryImportance of the HPC

Examination

Investigation

HistoryImportance of the HPC

Examination

Investigation

SymptomsSymptoms

DyspnoeaChest painHaemoptysis


SymptomsSymptoms



Dyspnoea: Pattern of Onset

Dyspnoea: Pattern of Onset

SuddenPneumothoraxPTEAspirationCardiac event –arrhythmia, MI

Over hours / daysAsthmaPneumoniaPulmonary oedema

SuddenPneumothoraxPTEAspirationCardiac event –arrhythmia, MI

Over hours / daysAsthmaPneumoniaPulmonary oedema

IntermittentAsthmaHyperventilation

ProgressiveCOPDIPFPleural effusionAnaemiaLVF Pulmonary hypertension

IntermittentAsthmaHyperventilation

ProgressiveCOPDIPFPleural effusionAnaemiaLVF Pulmonary hypertension

SymptomsSymptoms



Chest PainChest Pain

Myocardial ischaemiacentral radiating to the jaw / arm(s)squeezing / crushing / heavy weightaggravated by exertionrelieved by rest / GTNassociated autonomic features

Myocardial ischaemiacentral radiating to the jaw / arm(s)squeezing / crushing / heavy weightaggravated by exertionrelieved by rest / GTNassociated autonomic features


Myocardial ischaemiaPericardial pain

retrosternalpleuriticrelieved by sitting forwardworse on swallowing, twisting and with sternal pressure

Myocardial ischaemiaPericardial pain

retrosternalpleuriticrelieved by sitting forwardworse on swallowing, twisting and with sternal pressure


Myocardial ischaemiaPericardial painRespiratory

typically not centralpleuritic

Myocardial ischaemiaPericardial painRespiratory

typically not centralpleuritic


Myocardial ischaemiaPericardial painRespiratoryOesophageal

retrosternalheart burncan be indistinguishable from cardiac pain

Myocardial ischaemiaPericardial painRespiratoryOesophageal

retrosternalheart burncan be indistinguishable from cardiac pain


Myocardial ischaemiaPericardial painRespiratoryOesophagealMusculoskeletal

localisedassociated with tenderness

Myocardial ischaemiaPericardial painRespiratoryOesophagealMusculoskeletal

localisedassociated with tenderness

SymptomsSymptoms



HaemoptysisHaemoptysis

0

5

10

15

20

25

Perc

enta

ge o

f cas

es

Neoplasms

Bronchiectasis

Miscellaneous

Bronchitis

BacterialpneumoniaTuberculosis

Cryptogenic

Misc – PTE, LVF, aspergilloma, lung abscess, atypical mycobacteria

Other Points from the History

Other Points from the History

Don’t overlook the rest of the historyPMH - e.g. previous DVTDrug history - e.g. new medicationsSmokingOccupation e.g. baker, asbestos exposurePets especially birdsFH

Don’t overlook the rest of the historyPMH - e.g. previous DVTDrug history - e.g. new medicationsSmokingOccupation e.g. baker, asbestos exposurePets especially birdsFH

ExaminationExamination

Do not make the diagnosis from the history aloneIt is negligent not to examine a patient with new symptomsE.g. arrhythmia (esp AF / flutter)

pneumothoraxpericardial effusion

Do not make the diagnosis from the history aloneIt is negligent not to examine a patient with new symptomsE.g. arrhythmia (esp AF / flutter)

pneumothoraxpericardial effusion

ObservationsObservations

HR

BP

Temp

HR

BP

Temp

SpO2

FIO2

RR

SpO2

FIO2

RR

Examination of the Chest

ExpansionPercussionAuscultation

Air entryQuality of breath soundsAdded soundsVocal resonance

ExaminationExamination

WheezeAsthma / COPDHeart failureAnaphylaxisForeign body

StridorForeign bodyEpiglottitisAnaphylaxis

WheezeAsthma / COPDHeart failureAnaphylaxisForeign body

StridorForeign bodyEpiglottitisAnaphylaxis

CracklesPulmonary oedemaFibrosisPneumoniaBronchiectasis

Clear chestPTEPneumothoraxHyperventilationMetabolic acidosisAnaemiaDrug overdose

CracklesPulmonary oedemaFibrosisPneumoniaBronchiectasis

Clear chestPTEPneumothoraxHyperventilationMetabolic acidosisAnaemiaDrug overdose

InvestigationsInvestigations

Blood – FBC, U&Es, (D-dimer, Tn, CRP)ABGsECGCXR

Blood – FBC, U&Es, (D-dimer, Tn, CRP)ABGsECGCXR

ABGsABGs

Normal values

PaO2 10 – 13.3 kPaPaCO2 4.8 – 6.1 kPaH+ 35 – 45HCO3- 22 – 26 mmol/L

DoWrite the results in the notesDocument oxygen prescription

Normal values

PaO2 10 – 13.3 kPaPaCO2 4.8 – 6.1 kPaH+ 35 – 45HCO3- 22 – 26 mmol/L

DoWrite the results in the notesDocument oxygen prescription

Interpretation of Arterial Blood Gases

Interpretation of Arterial Blood Gases

PaCO2 PaCO2

H+

respiratory acidosis metabolic

acidosisrespiratory alkalosis

metabolic alkalosis

ABGsABGs

PaO2 7.0PaCO2 4.5 H+ 37HCO3- 25

PaO2 7.0PaCO2 4.5 H+ 37HCO3- 25

Type 1 respiratory failure

Type 1 respiratory failure

What are the physiological mechanisms for hypoxia?

ABGsABGs

PaO2 7.0PaCO2 8.0 H+ 55HCO3- 26

PaO2 7.0PaCO2 8.0 H+ 55HCO3- 26

Decompensated Type 2 respiratory failure

Decompensated Type 2 respiratory failure

What is the physiological mechanisms for hypercapnia?

ABGsABGs

PaO2 7.0PaCO2 8.0 H+ 41HCO3- 34

PaO2 7.0PaCO2 8.0 H+ 41HCO3- 34

Compensated Type 2 respiratory failure

Compensated Type 2 respiratory failure

ABGsABGs

PaO2 18.0PaCO2 1.7 H+ 22HCO3- 15

PaO2 18.0PaCO2 1.7 H+ 22HCO3- 15

HyperventilationHyperventilation

ABGsABGs

PaO2 18.0PaCO2 1.7 H+ 60HCO3- 10

PaO2 18.0PaCO2 1.7 H+ 60HCO3- 10

Metabolic acidosisMetabolic acidosis

ECGsECGs

When can they be helpful?

ArrhythmiaCardiac ischaemiaLVFPericardial effusionP.E.RVF / pulmonary hypertension

When can they be helpful?

ArrhythmiaCardiac ischaemiaLVFPericardial effusionP.E.RVF / pulmonary hypertension

CXRCXR

Case 1Case 1

62 ♀ Ex-smokerProgressive SOB over 18 monthsNow 4/7 SOB with productive cough

O/E SpO2 85% on air RR 30/minAE, minor wheeze, hyperinflated

62 ♀ Ex-smokerProgressive SOB over 18 monthsNow 4/7 SOB with productive cough

O/E SpO2 85% on air RR 30/minAE, minor wheeze, hyperinflated

Ix:

Bloods - WCCECG – normalABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3

- 26

CXR -

Ix:

Bloods - WCCECG – normalABGs - PaO2 5.5, PaCO2 7.8, H+ 50, HCO3

- 26

CXR -

DiagnosisDiagnosis

Exacerbation of COPD

Decompensated type 2 respiratory failure

Exacerbation of COPD

Decompensated type 2 respiratory failure

Outcome from Exacerbation of

COPD

Outcome from Exacerbation of

COPDUncomplicated exacerbation

79%Immediate intubation

1%

Resolve with nebuliser,controlled oxygen, etc

4%

NIV16%

Acidotic20%

Exacerbation of COPD100%

Men: 75/100,000/yrWomen: 57/100,000/yr Plant 2000

TreatmentTreatment

O

N

A

P

O

N

A

P

www.nice.org.uk/CG012NICEguideline

TreatmentTreatment

O Oxygen

N Nebulised bronchodilators

A Antibiotics

P Prednisolone

O Oxygen

N Nebulised bronchodilators

A Antibiotics

P Prednisolone

TreatmentTreatment

Nebulised Bronchodilators

Salbutamol 2.5 – 5mg as often as needed

Ipratropium bromide 500mcg 6 hourly

If patient is hypercapnic, the nebuliser should be driven by compressed air, not oxygen (to avoid worsening hypercapnia). If oxygen therapy is needed during the nebuliser, it should be administered simultaneously by nasal cannulae.

Nebulised Bronchodilators

Salbutamol 2.5 – 5mg as often as needed

Ipratropium bromide 500mcg 6 hourly

If patient is hypercapnic, the nebuliser should be driven by compressed air, not oxygen (to avoid worsening hypercapnia). If oxygen therapy is needed during the nebuliser, it should be administered simultaneously by nasal cannulae.

Evidence Level D

TreatmentTreatment

Antibioticsshould be used in exacerbations with purulent sputumHow many?

One – combination of amoxycillin / macrolide only used in pneumonia

First-line and second-line choicesdictated by likely organism

- S. pneumoniae, H. influenza, M. catarrhalisaminopenicillin or macrolide or tetracycline (NICE)(Coamoxiclav is a pretty safe first choice, Levofloxacin a useful second choice)

Antibioticsshould be used in exacerbations with purulent sputumHow many?

One – combination of amoxycillin / macrolide only used in pneumonia

First-line and second-line choicesdictated by likely organism

- S. pneumoniae, H. influenza, M. catarrhalisaminopenicillin or macrolide or tetracycline (NICE)(Coamoxiclav is a pretty safe first choice, Levofloxacin a useful second choice)

TreatmentTreatmentPrednisoloneconsider in patients admitted to hospital

Prednisoloneconsider in patients admitted to hospital

Cochrane Review 2005

TreatmentTreatment

Prednisolone

How much & for how long?30mg for 7-14 days (NICE) 40 – 50 mg for 1/52 (local practice)

Should you taper?Not if course less than 2-3 weeksPatients MUST be given clear instructions about why, when and how to stop their steroids

Prednisolone

How much & for how long?30mg for 7-14 days (NICE) 40 – 50 mg for 1/52 (local practice)

Should you taper?Not if course less than 2-3 weeksPatients MUST be given clear instructions about why, when and how to stop their steroids

TreatmentTreatment

Other OptionsIV aminophylline – no evidence but often used in most severe casesDoxapram – remarkably effective in short term (hours) but mostly superseded by NIVITU – in this country rationed by limited provision of beds

Other OptionsIV aminophylline – no evidence but often used in most severe casesDoxapram – remarkably effective in short term (hours) but mostly superseded by NIVITU – in this country rationed by limited provision of beds

Principles of Treatment of Respiratory Failure


1. Hypoxia will kill you first

2. Acidosis will kill you later

1. Hypoxia will kill you first

2. Acidosis will kill you later



1. Correct Hypoxia to acceptable levelsO2 –

if Type 1 RF - aim for PaO2 > 10if Type 2 RF – give controlled O2 - aim for PaO27-8

2. If respiratory acidosis develops, support the respiratory muscles

NIV (BiPAP) - on medical wardintubation and IPPV - ICU(respiratory stimulants e.g. doxapram)

1. Correct Hypoxia to acceptable levelsO2 –

if Type 1 RF - aim for PaO2 > 10if Type 2 RF – give controlled O2 - aim for PaO27-8

2. If respiratory acidosis develops, support the respiratory muscles

NIV (BiPAP) - on medical wardintubation and IPPV - ICU(respiratory stimulants e.g. doxapram)

Oxygen Toxicity in COPDOxygen Toxicity in COPD

Oxygen Toxicity in COPDOxygen Toxicity in COPD

OxygenOxygen

Nasal cannulaStandard maskMask with reservoir bag

Nasal cannulaStandard maskMask with reservoir bag

Inspired oxygen concentration depends on patient’s minute ventilation – patient also breathes in an unknown amount of air

Inspired oxygen concentration depends on patient’s minute ventilation – patient also breathes in an unknown amount of air

2-4L/min 25-40%

5-15L/min <50%

15L/min <70%

Controlled Oxygen Therapy


Venturi (Valve) MasksDeliver a high flow of a

mixture of oxygen and entrained air of known composition provided flow rate of oxygen is set correctly (specified on mask)

Venturi (Valve) MasksDeliver a high flow of a

mixture of oxygen and entrained air of known composition provided flow rate of oxygen is set correctly (specified on mask)



Venturi (Valve) MasksWorks by Bernoulli’s

principle – if oxygen speeds up its pressure drops and a large quantity of air is sucked in

Venturi (Valve) MasksWorks by Bernoulli’s

principle – if oxygen speeds up its pressure drops and a large quantity of air is sucked in



Venturi (Valve) MasksWorks by Bernoulli’s principle –

if oxygen speeds up its pressure drops and a large quantity of air is sucked in

The patient is surrounded by a bubble of air/oxygen of known concentration

Venturi (Valve) MasksWorks by Bernoulli’s principle –

if oxygen speeds up its pressure drops and a large quantity of air is sucked in

The patient is surrounded by a bubble of air/oxygen of known concentration

40% O2

Non-invasive VentilationNon-invasive Ventilation

= ventilation without an ET tube

avoidsventilator associated pneumonianeed for an ITU bed

allowsintermittent supportnormal eating, drinking, communication

= ventilation without an ET tube

avoidsventilator associated pneumonianeed for an ITU bed

allowsintermittent supportnormal eating, drinking, communication

NIV/BiPAPNIV/BiPAPHow is it given?

NIV/BiPAPnon-invasive ventilation/bilevel positive

airway pressure

NIV/BiPAPnon-invasive ventilation/bilevel positive

airway pressure

What is it?

Pressure

Time

4cmH2O

Inspiration Expiration12cmH2O

NIV/BiPAPNIV/BiPAPHow is it given?By a tight-fitting mask

attached to an NIV machine.

Typically an air compressor BiPAP with O2 supply direct to mask (%O2would then be limited to ~45-50%) but can be an ICU type ventilator (up to 100% O2)

How is it given?By a tight-fitting mask

attached to an NIV machine.

Typically an air compressor BiPAP with O2 supply direct to mask (%O2would then be limited to ~45-50%) but can be an ICU type ventilator (up to 100% O2)

Case 2 Case 2

65 ♀ PMH: IPFSudden onset of left-sided pleuritic chest painO/E Dyspnoeic at rest RR 30/minBibasal crackles R>L

65 ♀ PMH: IPFSudden onset of left-sided pleuritic chest painO/E Dyspnoeic at rest RR 30/minBibasal crackles R>L

Case 2Case 2

Ix:

Bloods – Normal including D-dimer

ABGs PaO2 7, PaCO2 4.5,…

ECG – normal

CXR -

Ix:

Bloods – Normal including D-dimer


ECG – normal

CXR -

Case 1Case 1

PneumothoraxPneumothoraxDefn: Air in the pleural spacePrimary – no associated lung disease (subpleural bleb)Secondary – associated lung disease (typically fibrosis or emphysema)No of hospital admissions:

Men 16.7 / 100 000 / yr (approx 250 in Greater Glasgow)Women 5.8 / 100 000 /yr

Smoking is the greatest risk factor12% lifetime risk in smokers (cf 0.1% in non-smokers)

Half recur within 4 years

Defn: Air in the pleural spacePrimary – no associated lung disease (subpleural bleb)Secondary – associated lung disease (typically fibrosis or emphysema)No of hospital admissions:

Men 16.7 / 100 000 / yr (approx 250 in Greater Glasgow)Women 5.8 / 100 000 /yr

Smoking is the greatest risk factor12% lifetime risk in smokers (cf 0.1% in non-smokers)

Half recur within 4 years

BTS Guidelines 2003

Volume of PneumothoraxVolume of Pneumothorax

Volume of PneumothoraxVolume of Pneumothorax

Small – visible rim of < 2cm

Large – visible rim of ≥ 2cm

Small – visible rim of < 2cm

Large – visible rim of ≥ 2cm

Treatment 1Treatment 1

Treatment 2Treatment 2

AspirationAspiration

X

+ +

Chest DrainChest Drain


X


Complications of Chest Drain

Complications of Chest Drain

Penetration of lung, stomach, spleen, liver, heart, great vesselsPleural infection (1%)Surgical emphysema (malpositionedtube or kinked/blocked tube)

Penetration of lung, stomach, spleen, liver, heart, great vesselsPleural infection (1%)Surgical emphysema (malpositionedtube or kinked/blocked tube)

Myths DebunkedMyths Debunked

Are expiratory films useful?Does high flow oxygen work?Should we clamp drains before removal?Are large drains better than small drains?What is first-line management of a tension pneumothorax?

Are expiratory films useful?Does high flow oxygen work?Should we clamp drains before removal?Are large drains better than small drains?What is first-line management of a tension pneumothorax?

NoYesNo (?)

No

NoYesNo (?)

No

Tension PneumothoraxTension Pneumothorax

Intrapleural pressure exceeds atmospheric due to one-way valve effect – results in venous return,

cardiac output, BPPatient rapidly distressed –sweating, cyanosis, HR, RR, EMD/PEA arrest

Intrapleural pressure exceeds atmospheric due to one-way valve effect – results in venous return,

cardiac output, BPPatient rapidly distressed –sweating, cyanosis, HR, RR, EMD/PEA arrest


Not dependent on the size of the pneumothorax


Treatment

Cannula of at least 4.5cm length in 2nd

ICS MCL

Treatment


ICS MCL

X


Treatment


ICS MCL

then

Chest drain

Treatment


ICS MCL

then

Chest drain

Case 3Case 3

35 ♂ PMH: UCSudden onset of SOB 3/7 agoProductive cough and left sided pleurisy for 2/7

O/E pyrexialLeft basal crackles and dullness

35 ♂ PMH: UCSudden onset of SOB 3/7 agoProductive cough and left sided pleurisy for 2/7

O/E pyrexialLeft basal crackles and dullness

Ix:

Bloods - WCC; D-dimerECG – normalABGs - PaO2 9.0, PaCO2 5.3, …

CXR –

Ix:

Bloods - WCC; D-dimerECG – normalABGs - PaO2 9.0, PaCO2 5.3, …

CXR –

Diff Δ:-PTEPneumonia

Diff Δ:-PTEPneumonia

Pulmonary EmbolismPulmonary Embolism

Annual incidence – 60-70 / 100 000 / yr 1000 in Greater Glasgow

Typically PTE is present in 15 – 40% of cases where the diagnosis is consideredModern diagnostic pathway uses:-

clinical probabilityD-dimer assayCTPA

Annual incidence – 60-70 / 100 000 / yr 1000 in Greater Glasgow

Typically PTE is present in 15 – 40% of cases where the diagnosis is consideredModern diagnostic pathway uses:-

clinical probabilityD-dimer assayCTPA

Pulmonary EmbolismPulmonary EmbolismDiagnostic Pathway

PIOPED II AJM 2006

Clinical Probability

Clinical Probability

Risk of PTE

BTS Guidelines 2003

Clinical Probability ScoresClinical Probability Scores

PIOPED II AJM 2006

Revised Geneva ScoreRevised Geneva Score

D-dimer AssayD-dimer Assay

Quantitative ELISA based assays (e.g. VIDAS) have sensitivity of ~ 95%But specificity poor

The only useful D-dimer result is a negative one

Chance of having had a PTE with negative D-dimer is

low clinical probability 0.7 – 2%moderate clinical probability 5%high clinical probability >15%

Quantitative ELISA based assays (e.g. VIDAS) have sensitivity of ~ 95%But specificity poor

The only useful D-dimer result is a negative one

Chance of having had a PTE with negative D-dimer is

low clinical probability 0.7 – 2%moderate clinical probability 5%high clinical probability >15%

PIOPED II AJM 2006

D-dimer AssayD-dimer Assay

It should not be done:-As a screening test on all general medical patientsIn high probability cases

It should not be done:-As a screening test on all general medical patientsIn high probability cases

ImagingImaging

CTPArapidly becoming the first line testsensitivity may be as low as 83% (PIOPED II NEJM 2006)

however, safe to withhold anticoagulation if CTPA negative (prevalence of further event by 3/12 ~ 1.5%) in low/moderate riskdebate as to best practice in CTPA –ve / high risk patientsvery useful for revealing alternative diagnoses

V/Qa useful alternative where CT contraindicated (e.g. iodine allergy) – generally only useful if CXR normal and no chronic cardiorespiratory disease

CTPArapidly becoming the first line testsensitivity may be as low as 83% (PIOPED II NEJM 2006)

however, safe to withhold anticoagulation if CTPA negative (prevalence of further event by 3/12 ~ 1.5%) in low/moderate riskdebate as to best practice in CTPA –ve / high risk patientsvery useful for revealing alternative diagnoses

V/Qa useful alternative where CT contraindicated (e.g. iodine allergy) – generally only useful if CXR normal and no chronic cardiorespiratory disease

TreatmentTreatmentLMW heparin

Difficulties arise with - obese patients- renal failure- rapid reversal

Oral anticoagulation with warfarinAim for INR of 2 – 3

Duration of anticoagulationTemporary risk factors 4-6/52Idiopathic 3-6/12

Risk of major bleeding≤ 3% at 3/12mortality ≤ 0.5%

Investigation for cancer usually unnecessary

LMW heparinDifficulties arise with

- obese patients- renal failure- rapid reversal

Oral anticoagulation with warfarinAim for INR of 2 – 3

Duration of anticoagulationTemporary risk factors 4-6/52Idiopathic 3-6/12

Risk of major bleeding≤ 3% at 3/12mortality ≤ 0.5%

Investigation for cancer usually unnecessaryBTS Guidelines 2003

Massive PTEMassive PTE

A pulmonary embolism so large as to cause circulatory collapseUsually the patient has presented with clear acute event often with syncope and is in extremisSigns of right heart failure with hypoxia i.e. BP, JVP, RV gallop, clear chest

A pulmonary embolism so large as to cause circulatory collapseUsually the patient has presented with clear acute event often with syncope and is in extremisSigns of right heart failure with hypoxia i.e. BP, JVP, RV gallop, clear chest

Investigation of massive PTE

Investigation of massive PTE

If patient peri-arrest, do not delay treatment for investigationsIf patient unstable, consider a cardiac echo (looking for RV dilatation) as first-line testIf patient stabilises, proceed to CTPA

If patient peri-arrest, do not delay treatment for investigationsIf patient unstable, consider a cardiac echo (looking for RV dilatation) as first-line testIf patient stabilises, proceed to CTPA

Treatment of Massive PTETreatment of Massive PTE

Thrombolysis

BTS Guidelines 2003

Other Treatment OptionsOther Treatment Options

Clot fragmentation by pulmonary artery catheter / interventional radiology

Embolectomy

Clot fragmentation by pulmonary artery catheter / interventional radiology

Embolectomy

How does a PE make you hypoxic?

When would you giveiv heparin?thrombolysis?an IVC filter?

How long should you anticoagulate?

Should you investigate for cancer?

How does a PE make you hypoxic?

When would you giveiv heparin?thrombolysis?an IVC filter?

How long should you anticoagulate?

Should you investigate for cancer?

D-dimerD-dimer

Sensitive but not specific test for VTEAllows you to rule out PTE or DVT in patients with low / moderate clinical probability (VIDAS assay)It should not be done:-

As a screening test on all general medical patientsIn high probability cases

Only useful if negative

Sensitive but not specific test for VTEAllows you to rule out PTE or DVT in patients with low / moderate clinical probability (VIDAS assay)It should not be done:-

As a screening test on all general medical patientsIn high probability cases

Only useful if negative

Clinical ProbabilityClinical Probability

In a patient with clinical features of PTE (sudden onset SOB, chest pain, haemoptysis…..)

a) Is there no other reasonable clinical explanation?

b) Is there a major risk factor?

a AND b HIGH a OR b but not both MEDIUMneither a nor b LOW

In a patient with clinical features of PTE (sudden onset SOB, chest pain, haemoptysis…..)

a) Is there no other reasonable clinical explanation?

b) Is there a major risk factor?

a AND b HIGH a OR b but not both MEDIUMneither a nor b LOW

Case 2Case 2

45 ♀SOB over several months

Worse at night, disturbing sleepWheezy at times with productive coughSon recently acquired pet rat

O/E Speaking in short sentencesHR 120/min RR 30/minPEF – not recorded Sp02 93% on airWidespread wheeze

45 ♀SOB over several months

Worse at night, disturbing sleepWheezy at times with productive coughSon recently acquired pet rat

O/E Speaking in short sentencesHR 120/min RR 30/minPEF – not recorded Sp02 93% on airWidespread wheeze

Ix:

Bloods – normal

ECG – normal


CXR

Ix:

Bloods – normal

ECG – normal


CXR

CXRCXR

How severe?How severe?

Severity of Acute AsthmaSeverity of Acute Asthma

Treatment of Acute Asthma




Anaphylaxis caseAnaphylaxis case

Correction of Hypoxia and Hypercapnia

Correction of Hypoxia and Hypercapnia

Correct hypercapnia by increasing alveolar ventilationCorrect hypoxia by reducing shunt i.e. you need to improve O2 delivery or decrease blood supply to diseased areas

Correct hypercapnia by increasing alveolar ventilationCorrect hypoxia by reducing shunt i.e. you need to improve O2 delivery or decrease blood supply to diseased areas

Uncontrolled OxygenUncontrolled Oxygen

2

20

2

10

Time

Flow

2L/min by nasal cannula does not necesssarily give 28%

Uncontrolled OxygenUncontrolled Oxygen

2

20

2

10

Time

Flow

2L/min by nasal cannula does not necesssarily give 28%

24% 35%

Documents

Acute Respiratory Emergencies · 2019-07-19 · Pneumothorax PTE Aspiration ... Modern diagnostic pathway uses:- clinical probability D-dimer assay CTPA. Pulmonary Embolism Diagnostic